Clinical Case Scenario

A 55-year-old woman with a history of severe alcohol use disorder and poor nutritional intake is brought to the ICU after a generalized tonic–clonic seizure. She is post-ictal but protecting her airway.

On examination, she appears markedly malnourished and is confused but conscious.

POCUS findings:

• Bilateral lung A-profile
• Preserved cardiac contractility on eyeball assessment
• Collapsing IVC

Vital signs:

• BP: 105/65 mmHg
• HR: 112/min

Laboratory Finding

• Sodium: 106 mmol/L
• Potassium: 1.8 mmol/L
• Chloride: 72 mmol/L
• Bicarbonate: 26 mmol/L
• BUN: 8 mg/dL
• Creatinine: 0.4 mg/dL
• Serum osmolality: 222 mOsm/kg
• Urine osmolality: 450 mOsm/kg
• Urine sodium: 12 mmol/L

She receives a 150 mL bolus of 3% hypertonic saline, after which her seizures cease.

Given her extremely high risk for osmotic demyelination syndrome (ODS), you plan to limit the serum sodium rise to ≤6 mmol/L during the first 24 hours.

The next priority is aggressive intravenous potassium chloride replacement for profound hypokalaemia.

Wrong Answer: ❌ A. It lowers serum sodium as administered potassium stimulates ADH release, leading to increased free-water retention.

Wrong Answer: ❌ A. It lowers serum sodium as administered potassium stimulates ADH release, leading to increased free-water retention.

Right Answer: ✅ B. It will increase serum sodium because retained potassium increases the total exchangeable cations, shifting sodium out of the cells to maintain electroneutrality.

Explanation

This question highlights an important yet frequently overlooked principle in the management of severe hyponatraemia with concurrent hypokalaemia.
The Edelman equation demonstrates that serum sodium concentration is a function of total body exchangeable sodium (eNa+), total body exchangeable potassium (eK+), and total body water (TBW):

Potassium behaves as an effective osmole just like sodium.
When intravenous potassium is administered:
• Potassium is rapidly taken up into the cells.
• To preserve electroneutrality, intracellular sodium moves into the extracellular space while hydrogen ions may also shift out of cells.
• Because potassium contributes to the pool of exchangeable cations, potassium replacement raises the serum sodium concentration, even without giving additional sodium.
Consequently, potassium repletion itself contributes to sodium correction.
This effect is particularly important in patients at very high risk of osmotic demyelination syndrome, including those with:
• Severe chronic hyponatraemia (especially Na⁺ <105 mmol/L)
• Alcohol use disorder
• Malnutrition
• Liver disease
• Profound hypokalaemia
Failure to account for the sodium-raising effect of potassium replacement can result in unintentional overcorrection of serum sodium, substantially increasing the risk of osmotic demyelination syndrome.

CLINICAL PEARLS

💎Potassium is not "sodium-neutral."
💥In severe hyponatraemia, every millimole of retained potassium contributes to the rise in serum sodium.
💥Potassium replacement should therefore be incorporated into the overall sodium correction strategy, with close monitoring to avoid exceeding the recommended correction limits.

Wrong Answer: ❌ C. It lowers serum sodium because activation of the Na⁺/K⁺-ATPase pump drives sodium into cells during potassium replacement.

Wrong Answer: ❌ D. It has no clinically meaningful effect on serum sodium, provided potassium is administered in 0.45% saline.